Seizures are the most common clinical manifestation of cerebral cysticercosis and occur in the presence of viable, dying, and calcified or noncalcified dead cysts. How calcified cysts provoke seizures is not known but recent observations demonstrated edema around some calcified lesions at the time of seizure activity and disappearance during periods when seizures were not occurring. Edema associated with foci in idiopathic epilepsy is highly unusual so that this observation suggests that the mechanism(s) associated with calcified cysts is unique. Documenting and understanding this phenomenon is important for a number of reasons. First, although by definition these lesions are inactive, e.g., not living larvae and do not require anti- parasitic treatment, they are frequently mistaken for active lesions and patients undergo unnecessary treatment. Second, a likely reason for perilesional edema is intermittent antigen release and subsequent host immune response resulting in inflammation and edema. If proven, then the treatment for this would not only involve suppression of seizure activity with anti- seizure medication, but also the use of anti-inflammatory medications such as corticosteroids. A study was initiated in Peru to determine 1) the frequency of perilesional edema around calcifications 2) the frequency of associated symptoms 3) what lesions and patients have a propensity to undergo this phenomenon 4) the natural history of perilesional edema and 5) whether treatment of patients with perilesional edema with corticosteroids results in enhanced regression of edema and clinical benefit. During accural of patients to perform the above study, a baseline MRI was obtained in patients with or without current symptoms. Thirty-four and one-half percent showed perilesional edema. This is a minimal estimate but shows that perilesional edema is common in endemic regions and is likely one of the most common causes of morbidity due to neurocysticercosis in this population.